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30 ESOPHAGEAL DYSMOTILITY IN EOSINOPHILIC ESOPHAGITIS: ANALYSIS USING HIGH-RESOLUTION ESOPHAGEAL MANOMETRY.
  1. J. Chen,
  2. S. K. Ghosh,
  3. J. Pandolfino,
  4. P. J. Kahrilas,
  5. I. Hirano
  1. Northwestern University, Chicago, IL.

Abstract

Background Eosinophilic esophagitis (EE) is an increasingly recognized cause of dysphagia and food impaction. In many cases, strictures are not apparent on endoscopy, raising questions as to the mechanism of impaired deglutition. Prior reports have documented eosinophilic infiltration of the muscularis propria and myenteric plexus that could induce esophageal dysmotility.

Aim Characterize esophageal motor function in EE using high-resolution esophageal manometry (HRM) and newly described manometric parameters.

Methods Twenty-four patients with EE were studied with a 36-channel solid-state HRM assembly and analyzed using ManoView software (Sierra Scientific). Analysis was based on 10 5 mL water swallows per patient. Esophageal peristalsis was quantified by distal esophageal body peristaltic point velocity and pressurization front velocity (PFV), which was the propagation rate of an intact 30 mm Hg pressure wave. In the absence of a continuous propagation wave, a swallow was classified as a null PFV. A patient was classified as null, normal, or elevated PFV based on the dominant pattern (6) of 10 swallows. Esophagogastric junction (EGJ) relaxation was quantified using the lowest mean residual pressure over a 3-second interval (E-sleeve relaxation) and integrated relaxation resistance (IRR). A higher IRR signifies impaired EGJ relaxation and consequently higher resistance to esophageal emptying. All abnormal HRM values were referenced to the 95% upper limit of normal values derived from 75 controls.

Results The median patient age was 42 years (range 14-80 years). The most common presenting symptoms were dysphagia (83%) and heartburn (12.5%). Endoscopic findings included rings (50%), furrows (58%), and exudates (33%). On HRM, 14 patients (58%) had increased distal segment contraction velocity (median 8.4 cm/s), whereas 3 patients (12%) had an elevated PFV (median 4.2 cm/s). Two patients had elevated intrabolus pressures as evidenced by an elevated PFV but normally propagated peristaltic contraction. Nine patients were classified as having a null PFV and only one had significantly elevated esophageal contractile pressures (295 mm Hg). Seven patients had an elevated IRR (median 3.3 mm Hg/s), and of this group, 5 patients also had increased E-sleeve relaxation pressures (median 18 mm Hg).

Conclusions (1) Manometric manifestations of EE are heterogeneous. (2) An elevation in esophageal peristaltic velocity was the most common abnormality. (3) Subsets of EE patients demonstrated failed esophageal peristalsis (null PFV) and impaired EGJ relaxation (elevated IRR). (4) Functional abnormalities on the basis of neuromuscular involvement could contribute to dysphagia in EE.

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